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    (0025.7974/78/5704.0887802, 00/0 Mrpicine Copyright © 1978 by The Williams & Wilkins Co ‘Vol. 87, No. 4 Printed in USA CARDIAC RISK FACTORS AND COMPLICATIONS IN NON-CARDIAC SURGERY LEE GOLDMAN, M.D., DEBRA L. CALDERA, R. R. NUSSBAUM, M.D., BARBARA MURRAY, M. GOROLL, M.D., CHARLES H. CAPLAN, M. DONALD KROGSTAD, M.D., BLASE CAR: INTRODUCTION Several reports have shown that myocardial infarction occurs after about 0.15 percent of operations in adults (14, 35, 53). In patients with a history of a prior infarction (2, 3, 538, 55), angina (10), or arteriosclerotic heart disease (2, 10), most estimate that the risk of postoperative infarction increases to about 6%, and that over- all mortality also increases (33, 49). However, in one study (13) a cardiac death rate of less than 1% was noted even in patients with an- gina or old infarctions. There is similar disa- greement on whether prolonged intraoperative hypotension predisposes cardiac patients to postoperative infarction (29, 46), but all seem to agree that patients are at greatest risk in the first 6 months after an infarction (2, 10, 15, 53, 55). A major factor in the variability of reported results is the way in which patients are evalu- ated postoperatively. For example, Driscoll (12) showed a 2% incidence of clinically silent in- farctions when routine postoperative electro- cardiograms (EKG’s) were obtained. One limitation of previous studies of cardiac risk in non-cardiac surgery is that they were conducted prior to 1970. Since then, the in- creased anesthetic experience in patients un- dergoing coronary artery bypass surgery might be expected to lead to a reduction in periopera- tive cardiac complications. Second, the retro- spective univariate analysis of previous studies has ignored the potential interrelations among various risk factors. Because of these limita- From the Departments of Medicine and Anesthe- siology, Massachusetts General Hospital, Boston, Massachusetts 02114. ‘This study was supported by the Francis C. Man- ning Fund of the Medical Services of the Massachu- setts General Hospital. Address correspondence to Lee Goldman, M.D., Section of Cardiology, 87 LMP, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06510. No reprints will be made available to the general readership. N., FREDERICK S. SOUTHWICK, M.D., SAMUEL D., TERRENCE A. O'MALLEY, M.D., ALLAN H. JAMES NOLAN, M.D., DONALD S, BURKE, M.D., ABELLO, M.D., ano EVE E. SLATER, M.D. tions, a prospective study of cardiac risk factors in non-cardiac surgery was begun in the fall of 1975. METHODS Between October 1975 and April 1976, 1001 con- secutive patients over the age of 40 (including 651 ward general surgery, orthopedic surgery, and uro- logic surgery patients and 350 private general sur- gery, vascular surgery, gynecologic surgery, and urologic surgery patients) who had procedures other than transurethral prostatic resection or uncompli cated endoscopy were entered into this study. Each patient was seen preoperatively or, in occasional cases of emergency late-night surgery, as soon possible postoperatively by one of the senior medical resident co-authors. Each, patient was specifically questioned about any history of chest pain, short- ness of breath, orthopnea, edema, hypertension, hyperlipidemia, tobacco use, diabetes, myocardial infarction, congestive heart failure or arrhythmias. New York Heart Association functional class was determined from an assessment of symptoms. All present or past cardiac or antihypertensive medica- tions were recorded. Each patient received a de- tailed cardiac examination including auscultation of the heart and lungs, palpation of peripheral pulses, observation of the jugular venous pulsations, and examination of the extremities. All available pa- tient records were reviewed in detail for corrobor tion of historical and examination findings and to see whether any other cardiac abnormalities had been present in the past. Preoperative vital signs were recorded. Each patient had a preoperative el trocardiogram (EKG) and chest x-ray officially in- terpreted by the appropriate hospital department, Other pertinent laboratory data such as rengl and liver function tests, hematocrit, and, when availa- ble, arterial blood gases and pulmonary function tests were tabulated. All data were recorded on # five-page computer-coded form by the senior resi- dent who examined the patient. All patients were informed of the study's design and goals, Of the 1002 patients offered entry into the study, only one refused. Each patient's operative course was recorded. Every patient had continuous electrocardiographic monitoring in the operating 357 358 room. Blood pressure was recorded by arm cuff ‘measurement, usually every five minutes. Each of the 651 ward patients was followed post: operatively on a surgical service which had a senior medical resident co-author acting as full-time con- sultant, Medically unstable patients were seen daily by the medical senior resident. Others were always seen if they developed cardiac signs, symptoms, or EKG changes. Private patients were seen at least ‘once postoperatively by one of us (L.G.), and were ‘seen whenever cardiac signs or symptoms or EKG changes developed. Patients’ charts were reviewed daily during hospitalization and in detail after dis- charge by one of us (L.G.) Whenever a patient developed cardiac signs or symptoms or was thought by his physicians to have any potential cardiac problem, an EKG or serial EKG's were performed. In addition to any clinically indicated EKG's, each patient had a protocol postop- erative EKG on about the fifth postoperative day; the protocol EKG's were performed sooner if the patient's projected hospital stay was less than 5 days, and they could not be performed on weekends, Cardiac enzymes were studied whenever a patient complained of chest pain or had any changes on physical examination or EKG which raised the clin: ical question of a myocardial infarction. ‘Any postoperative cardiac complication which de- veloped prior to discharge or death was recorded. A postoperative transmural myocardial infarction was diagnosed if the patient developed new Q waves which were at least 0.04 seconds in duration and one millimeter or more in depth, In our series, these Q waves were almost always associated with new ST elevation. The diagnosis of a nontransmural my- ‘cardial infarction required new ST segment depres- sion or T wave inversion which either (a) were asso- ciated with chest pain typical of myocardial is- chemia, persisted for at least 72 hours, and could not be explained on the basis of medications or electro: lyte imbalance, (b) were associated with elevations of SGOT, CPK or, when available, CPK isoenzymes out of proportion to surgery itself, or (©) persisted as new ST depressions of 1 mm or more and symmetri- cal T wave inversion for at least 7 days without other explanation, Any questionable diagnoses were reviewed by independent cardiology observers. Heart failure was diagnosed if the patient devel- ‘oped new signs of pulmonary congestion on physical examination, a new S, gallop, or a diagnostic chest x-ray; only patients who had new congestive heart failure or a worsening of old congestive heart failure such that new or increased medications were re- quired were considered to have postoperative congestive heart failure. Pulmonary edema was di- agnosed if a patient had a classic chest x-ray or developed respiratory distress at rest and rales at least three-fourths of the way up his lung fields. Supraventricular arrhythmias required a diagnostic GOLDMAN ET AL. electrocardiogram for review; the only exceptions were intraoperative arrhythmias, especially brady- arrhythmias, which were seen on continuous elec- trocardiographic monitoring and could not be veri fied by formal electrocardiograms. A cardiac death was diagnosed if a patient died either from an ar- rhythmia or with refractory low-output cardiac fail- ture, as verified by the thermodilution technique, which was not part of an inexorable downhill course primarily caused by some non-cardiac condition such as sepsis, respiratory failure or metastatic ma- lignaney. A non-cardiac death was defined as death from any other cause, regardless of whether or not, there was an associated cardiac condition or compli cation. Except where otherwise indicated, significance testing was performed by Chi-square analysis. RESULTS Table 1 shows the distribution of the 1001 operations in this series. All operations were considered to be major surgical procedures; 866 were performed with general anesthesia, 116 were performed under spinal or epidural anes- thesia, and only 19 were extensive operations performed under local or regional anesthesia. Incidence of postoperative infarction and cardiac death Fifty-nine patients died prior to hospital dis- charge; 19 of these were cardiac deaths. Of the 18 diagnosed postoperative myocardial infare- tions, the 11 transmural infarcts resulted in 4 cardiac deaths, while the 7 nontransmural in- farets resulted in 1 cardiac death. Nine of the infaretions were associated with pain. Of the nine painless infarctions, eight were diagnosed by the patients’ own physicians when they pre- sented with one or more cardiac symptoms other than pain: new or markedly worsened congestive heart failure (five patients), hypo- tension (three patients), or new supraventricu- lar tachycardia (one patient). Fifty-one pa- tients developed transient postoperative ST segment or T wave changes suggestive of is- chemia but did not meet the criteria for a non- transmural infarction. Just one postoperative myocardial infarction was documented among, the 1001 patients only by the routine free pos operative electrocardiogram. Two of the infare- tions occurred intraoperatively, six more oc- curred within 3 days, and another eight ap- peared by day 6, ‘The mortality rate after a postoperative in- TABLE 1 Operations Included in This Study ‘Abdominal Total Mediastinos- Head, neck, superficial or copy, operation Perianal, Retroperito- neal, pelvic CARDIAC RISK FACTORS IN NON-CARDIAC SURGERY 359 ‘a endoscope extremity i Peripher aneurysm Type of operation vascula Thoracie Lower abdominal Upper abdominal 197 31 16 18 18 20 No. Emer- gency No, Elective Total 804 1001 m4 a 200 231 1 137 34 38 3 6 62 64 31 82 155 233 farction depends on how sudden deaths are classified and whether mortality statistics clude only cardiac deaths or all causes of death (Table 2). Fourteen patients died from cardiac causes without documented myocardial infarctions by electrocardiograms or autopsy: 5 had sudden cardiac deaths while another 9 patients died with refractory cardiogenic shock, with or with- out terminal arrhythmias. Overall, 11 of the 19 postoperative cardiac deaths were from cardi- ogenie shock whereas 8 were sudden from pre- sumed arrhythmias. Two cardiac deaths oc- curred in patients who had operations for car- diac symptoms which simulated emergency surgical conditions. One of these patients is discussed in Table 3. The other was a 70-year- old woman with severe congestive heart fail- ure, hypothyroidism, and liver distention whose right upper quadrant tenderness, hypo- tension, and hypothermia were mistakenly at- tributed to biliary sepsis, Recent preoperative myocardial infarction as a risk factor for postoperative infarction and cardiac death (Table 3) Cardiac death occurred in 5 of 22 patients (22.7%) who had had an infarction within 6 months preoperatively, but in only 2 of 79 pa- tients (2.5%, p < 0.001) whose prior infarct was more than 6 months preoperatively. The risk of cardiac death in the interval between 4 weeks and 6 months after a previous infarction was not significantly lower than that in patients within 4 weeks of their infarctions. Among those with infarets more than 6 months preop- eratively, the risk of cardiac death was no higher than in those who had never had an infarction (12 of 894 patients, 1.3%) There was no statistical correlation between interval since preoperative infarction and occurrence of a non- fatal postoperative infarct. Among the patients with operations less than 6 months after an infarction, there were 3 car- diac deaths and 1 nonfatal infaretion after the 11 emergency operations, and there were 2 car- diac deaths after the 11 elective procedures; none of the 22 patients died from non-cardiac causes. Two cardiac deaths and 1 nonfatal in- farction occurred in the 10 patients with a re- cent preoperative transmural infarction, while 3 cardiac deaths occurred in those 12 with a recent preoperative nontransmural infarction. 360 Correlates of postoperative myocardial infarction ‘Among all the various signs and symptoms of heart disease by history, physical examination, EKG, and chest x-ray, there were only five significant correlates of intraoperative or post- operative myocardial infarction: age over 70 years; shortness of breath, orthopnea, or edema; grade II/VI or louder murmur of mitral regurgitation; more than five PVC's per minute documented at any time preoperatively; and tortuous or calcified aorta on chest x-ray (see Appendix). Despite the paucity of statistically significant predictors of infarction, the 18 patients who developed postoperative infarcts were rarely to- tally without risk factors. Five of the 18 had a GOLDMAN ET AL. history of congestive heart failure and 7 had a history of ischemic heart disease. Overall, only 2 of the 18 patients with a postoperative my- cardial infarction had no symptoms of is- chemia, no history of congestive heart failure, and totally normal preoperative electrocardi- ograms. Correlates of postoperative cardiac death (see Appendix) Nearly every sign, symptom, and EKG crite- rion of heart disease had a statistically signifi- cant correlation with postoperative cardiac death. When comparing patients with a parti ular factor to those without it, the risk ratio for cardiac death for the subset with the signficant factor varied from about 5:1 for QRS more than ‘TABLE 2 _ Mortality from Postoperative Myocardial Infarction _ ~~ Number of Morality repo ——— & Overall rave Prnyocardial’ Cardiac Noneardiac Total "tality infarctions _ Pooled Series from Literature’ 42 12 52% Present Series, Documented Myocardial 18 5 3 8 4% Infarctions Present Series, if sudden probably ar- 2 10 3 13 51% thythmic deaths were considered as myocardial infarctions _ i "References 2, 3, 14, 33, 35, 53, 55, 60. TABLE 3 Relation between Previous History of Myocardial Infarction and Postoperative Infarction or Cardiac Death Portoperstive myocardial infarction” Cardiac death Hinory of previous my- No of pa Without doe teeiefarbn or cardial infarction” tient Non fatal Fatal -—-‘Total’_«=— mented in- Total’ —cardine death Taretion Not more than 4 weeks 12 1 0 18%) 3 325%) 433%) 6' weeks-8 months ago 10 ° o 0 2 2 (20%) 2 (20%) 6 months-2 years ago 13 ° o 0 1 18%) 18%) 2-5 years ago 53 1 1 24%) ° 12%) 24%) More than 5 years ago 13 0 0 0 ° ° 0 Never 804 u 4 5@%) 8 120%) 23 (8%) NS! p< .0or p< .001? Total tool 13 5 1808R) 199%) _—_—32. 2%) "There were no patients between 4 and 6 weeks after an infarction, * This one patient had had a documented myocardial infarction 8 months preoperatively. His present operation was for pain which was misdiagnosed as a leaking abdominal aortic aneurysm, but in retrospect was the presentation of a fatal myocardial infarction. + Significance level comparing patients leas than 6 months after a myocardial infarction to those who are either more than 6 months after an infarction or have never had one. There is no significant difference between those more than 6 months after an infarction and those who have never had an infarction. CARDIAC RISK FACTORS IN NON-CARDIAC SURGERY 0.08 seconds, ischemia by history or EKG, ab- normal ST segments, cardiomegaly by x-ray, abnormal T waves, atrial fibrillation, pulmo- nary rales, murmur of mitral regurgitation, or congestive heart failure despite treatment; to about 14:1 for significant aortic stenosis or his- tory of pulmonary edema; to about 20:1 for Sy gallop, rhythm other than normal sinus or atrial fibrillation, or definite jugular venous distention. Unless an S, gallop or jugular ve- nous distention was present on the preopera- tive cardiac examination, those patients with congestive heart failure despite treatment were at only marginally greater risk than those with a history of congestive failure who were no longer in failure at the time of operation. Pre- mature ventricular contractions (PVC’s) were significant only if they had been present at a frequency of more than five per minute at some time past or present. Nonspecific ST segments and T waves had as strong a correlation with cardiac death as did ischemic changes. Varia- bles not associated with significantly increased risk for cardiac death included hypertension (now or in the past, treated or untreated), gallops, systolic ejection murmurs without evi- dence of significant aortic stenosis by physical examination, abnormal aorta on x-ray, diabetes mellitus, hyperlipidemia, and body build, Of the 19 patients with postoperative cardiac deaths, 11 had well-documented ischemic heart disease (manifested by either angina or history of myocardial infarction), 7 had well-docu- mented congestive heart failure, and 6 were not in normal sinus rhythm. The three patients who died from cardiac causes but had none of the above abnormalities were each in their mid-70's and had other evidence of major heart disease. Congestive heart failure ‘The best predictors of new or significantly worsened postoperative heart failure and pul- monary edema are the signs and symptoms of preoperative heart failure (Table 4). New York Heart Association functional classification of symptoms of congestive heart failure was an excellent predictor of postoperative failure and pulmonary edema. Patients with a positive his- tory for heart failure who were no longer in failure preoperatively were significantly less likely to develop pulmonary edema than were 361 those whose congestive failure was still evident preoperatively. Neither angina nor recent or distant preoperative myocardial infarction was independently related to postoperative heart, failure. Although the number of patients is small, about 20% of patients with a) mitral regurgita- tion murmurs of grade II or louder (9 out of 47 patients), or b) physical examination findings or historical documentation of significant aortic regurgitation (3 out of 12 patients), significant mitral stenosis (4 out of 14 patients), or signifi- cant aortic stenosis (4 out of 23 patients) devel- oped new or worsening heart failure in the postoperative period. Among the 25 patients on propranolol preoperatively, only 1 developed postoperative heart failure; this risk was no different from control risk. Despite the correlation between preoperative and postoperative heart failure, 21 of the 36 patients who developed pulmonary edema had no prior history of congestive heart failure. All but 2 of these 21 patients were over 60 years of age. Seventeen of the 21, including both pa- tients under the age of 60, had either abdomi- na] aortic aneurysm repair or abdominal sur- gery. Two-thirds had more than nonspecific electrocardiographic abnormalities preopera- tively and only two had totally normal preoper- ative electrocardiograms. Six of these 21 pa- tients developed their pulmonary edema after postoperative myocardial infarctions. Overall, 40% of the 36 patients who developed cardio- genic pulmonary edema died cardiac deaths, and 17% died from other causes for an overall mortality of 57%. Similarly, of the 27 patients with recognized new or significantly worsened postoperative failure without progression to pulmonary edema, 16 had no prior history of heart failure. Age over 60 years and major operations were also common in this group, but no preoperative cardiac risk factors were useful predictors of new mild congestive failure. None of these pa- tients with a new onset of mild heart Tailure had postoperative infarctions, none died car- diac deaths, and only 15% died from all causes. Cardiac arrhythmias New intraoperative or postoperative supra- ventricular tachycardias (SVT) (including atrial fibrillation, atrial flutter, multifocal atrial tachycardia, paroxysmal atrial tachycar- 362 GOLDMAN ET AL. TABLE 4 Correlation between Preoperative Heart Failure and Worsened Postoperative Heart Failure or Pulmonary Edema ap isi ooeal cate. Sen sme mates als Frege ay Never ‘8 co “ rh fat Inpansnatnow we Tans dos 6 ws ts cannon (p< 01 fr Group tas < 016 Grp ce SSnpart tn Grog and pinto Grup 8 or itn 3 compart io Snmupzve Grupo) rap 2) Clie unions les Cn Ps 2 os as cine i i * Class 3 34 8% 18% Class 4 17 25% 31% (p= ,to1fr Cass 4con- (p<. fr Clases 182 fhritnaiee) pared to Cay for Class 4 compared to Cian Sopulr venous a we a slo 8 ave ow Hon” of pulmo 2 aa" oe nary edema Lata hart a we oe ture by exam or x: “All p's < 01 when comparing patients with the findings to those without it. dia, or supraventricular tachycardia of unclear type) were noted in 39 patients (3.9%). New SVT's were diagnosed in 10% of patients over the age of 70, 13% of patients whose exercise had been limited by congestive heart failure, 8% of those with preoperative pulmonary rales, 9% of those with changes of chronie obstructive pulmonary disease diagnosed by chest x-ray, and 7% of patients with abnormal ST or T waves on electrocardiogram (all p's = 0.05) ‘Twelve of the 39 patients with new SVT's were on digitalis, but none were on quinidine. ‘There were 111 bradyarrhythmias (52 epi- sodes of nodal rhythm and 59 instances of new sinus bradycardia below 60 per minute) noted in 104 patients. Seventy-one (62%) of these epi- sodes occurred in the operating room, and all but one of the others occurred in the postopera- tive recovery room. The bradyarrhythmias nearly uniformly were self-limited or responded rapidly to atropine or a brief beta-adrenergic challenge. Bradyarrhythmias occurred in 29% of the patients digitalized after hospital admis- sion, but in only 12% of patients who were on digitalis at the time of the admission. Heart block Among the 45 patients with bifascicular heart block (20 patients with left bundle branch block, 23 with right bundle branch block plus left anterior hemiblock, and 2 with a right bun- dle branch block plus left posterior hemiblock), including 7 patients who also had P-R intervals greater than 0.20 seconds, there were no in- stances of recognized complete heart block. On the other hand, 4 of the 14 patients with a history of second or third degree heart block died from cardiac causes without observed pro- gression to complete heart block. Blood pressure and surgery Preoperative hypertension was not an inde- pendent predictor of cardiac death, postopera- tive myocardial infaretion, heart failure, or ar- rhythmias. CARDIAC RISK FACTORS IN NON-CARDIAC SURGERY Patients with preoperative hypertension, re- gardless of whether they were on treatment or whether the treatment had normalized their blood pressures, were more likely to develop hypertension, as defined by a systolic pressure greater than 200 mm of mereury or more than 40 mm higher than preoperative blood pres- sure, intraoperatively or within 48 hours post- operatively (17% compared to 6% in previously normotensive patients; p < 0.01). Almost three- fourths of the episodes of postoperative hyper- tension occurred in patients who had vascular surgery, especially abdominal aortic aneurysm repair or carotid endarterectomy. Postoperative hypertension was not an independent predictor of any other postoperative cardiac complica- tion ‘Thirty-five patients had labile hypertension, defined as the presence of both hypertension (as defined above) and a 33% intraoperative drop in their systolic blood pressure. These patients were not at increased risk for any postoperative cardiac complications except for pulmonary edema (11% vs 2% for controls), and even that relationship lost its significance when con- trolled for preoperative congestive heart fail- ure. ‘The operation and the anesthetic technique Patients who had intra-abdominal, intra-tho- racic, or aortic operations were more likely to develop postoperative pulmonary edema (23 of 437 compared to 2 of 564, p < 0.001) and supra- ventricular tachycardias (28 of 437 compared to 13 of 564, p = .001). Although aortic operations were associated with the highest risk of postop- erative pulmonary edema (11%) and mild heart failure (an additional 9%), neither aortic nor peripheral vascular procedures to treat existing atherosclerotic problems carried an increased risk of postoperative infarction or cardiac death; in fact, these latter two cardiac compli- cations were independent of the type of opera- tion. Procedures which lasted more than 5 hours were associated with increased risk of heart failure and non-cardiac death but not cardiac death or infarction. None of the 11 patients who had controlled intraoperative hypotension had any cardiac sequelae. Although patients oper- ated on under spinal or epidural anesthesia were not statistically less likely to develop in- traoperative hypotension or perioperative car- 363 diac death than those receiving general anes- thesia, none of the spinal or epidural patients developed postoperative myocardial infarctions or heart failure. Among patients who had gen- eral anesthesia, there was no difference in the development of complications based on whether a patient received halothane, nitrous oxide, or other general anesthetics. Patients who had emergency procedures were four times as likely to develop postopera- tive infarctions or cardiac death (both p's < 0.01). Those who had unplanned systolic blood pressure reductions of 33% or more for greater than 10 minutes had a five-fold increased inci- dence of cardiae death (p < 0.05), but no greater risk of nonfatal postoperative infarction Multivariate analysis of correlates of cardiac death By multivariate regression analysis, the only factors which were independently correlated with postoperative cardiac death were: a) pres- ence of jugular venous distention or an S; gal- lop immediately preoperatively; b) a myocar- dial infarction in the preceding 6 months; c) rhythm other than sinus, or presence of prema- ture atrial contractions on preoperative EKG; 4) more than five premature ventricular contra- tions per minute documented at any time pre- operatively; e) evidence suggesting significant valvular aortic stenosis; f) age over 70 years; g) emergency operation; h) an unplanned 33% or greater reduction of systolic blood pressure for more than 10 minutes during the operation. DISCUSSION This is the largest prospective study of car- diac risk in non-cardiac surgery in which pa- tients were actually examined, Much of the limited previous data has been substantiated, but many facets have been more clearly eluci- dated Our finding of 50% painless infarets ig higher than the 20-40% usually quoted in the nonoper- ated general population (26, 30, 51), but very similar to the 53% incidence of painless postop- erative infarcts reported in 124 patients in 5 large series (12, 14, 35, 53, 60), We agree with previous studies (14, 35, 60) that the risk of postoperative infarction peaks at about day 5, but while others have described up to 35% in- farctions occurring in the operative room on the 364 day of surgery, only 2 of our 18 recognized infarctions occurred within 24 hours of the oper- ation. The improved anesthetic techniques gleaned from experience with cardiac surgery tay be a major explanation for this difference. ‘Though Driscoll (12) reported a 2% incidence of unsuspected myocardial infarction found by routine postoperative EKG's, with our close clinical follow-up and at least 1 EKG we noted only 1 such patient in 1001, and even that pa- tient died from cardiac causes despite the EKG. Since routine daily EKG’s and creatine kinase isoenzymes were not performed, we cannot, comment on the possible rate of clinically silent, (without pain, heart failure, hypotension, or observed arrhythmias) nontransmural infare- tions which might have resolved electrocardi- ographically by the time of the routine postop- erative EKG. Recent myocardial infarction as a risk factor for postoperative infarction and cardiac death Pooled series from the literature (2, 3, 10, 13, 15, 53, 55) show a 38% risk of cardiac death or recurrent infarction (usually fatal) in 151 pa- tients who were operated on when they were less than 6 months after a myocardial infare- tion. The 27% rate among our 2 patients is somewhat lower, but emphasizes the danger of operation in this subgroup. Tarhan (53) showed 37% (3 of 8) rate of reinfarction among pa- tients less than 6 weeks after an infarction and a 16% (3 of 19) rate of reinfarction among those 6 weeks to 6 months after an infarct. However, the difference between these subgroups in Tar- han's study, our study, or the two studies com- bined is not statistically significant. Arkins (2) described a much lower risk after nontrans- mural as compared to transmural infarction, but the similar risk we found in both subgroups agrees with the overall similarity in prognosis after nontransmural and transmural infare- tions (6, 28, 36, 43). Although Topkins and Ar- tusio (65) felt risk did not return to baseline until 2 years after an infarct, we agree with ‘Tarhan (53) that risk declines by 6 months. We recommend that non-emergent procedures be postponed for at least 4 to 6 weeks and prefera- bly a full 6 months after a transmural or a non- transmural myocardial infarction. Correlates of postoperative infarction In our patients, in whom at least subclinical atherosclerotic coronary vascular disease was GOLDMAN ET AL. probably usual, development of a postoperative ‘myocardial infarction was very difficult to pre- dict. Of all the variables analyzed, only five were significantly correlated with postopera- tive infarction and of those five only two (fre quent PVC’s and a murmur of mitral regurgi tation) carried more than a 4% risk. However, only two patients with absolutely no preopera- tive risk factors had postoperative infarctions Correlates of postoperative cardiac death As noted by others (2, 33, 49), patients with preoperative heart disease had higher perioper- ative mortality rates than those without heart. disease. In fact, each of our 19 patients who died from cardiac causes had evidence of ischemic heart disease, heart failure, abnormal rhythm, valvular heart disease, or major EKG abnor- malities. Although there were numerous uni- variate correlates of postoperative cardiac death, the lack of statistical significance of fac- tors such as angina, hypertension, smoking, known hyperlipidemia, diabetes mellitus, body build, compensated congestive heart failure, S, gallops, and systolic ejection murmurs without aortic stenosis is noteworthy. Congestive heart failure Although patients with preoperative heart failure were at highest risk for postoperative pulmonary edema, 58% of the 36 patients who developed pulmonary edema had no prior signs or symptoms of heart failure. Cooperman and Price, in a study of postoperative pulmonary edema, found a 1% incidence in all patients over the age of 1 year (9). Our rate was 3.6%, and though preoperative failure was the best predictor, age over 60 years, major opera- tion, and asymptomatic electrocardiographic changes were all correlated with the develop- ment of new pulmonary edema. The 57% mor- tality in our series is almost three times the mortality of the younger patient population re- ported by Coopermen and Price Six additional patients had pulmonary edema associated with sepsis and an elevated cardiac index by the thermodilution technique. These patients were felt to have non-cardi- ogenic pulmonary edema and are not included in the discussion above. Cardiac arrhythmias We observed new supraventricular tachyar- rhythmias (SVT's) after 10% of intrathoracic CARDIAC RISK FACTORS IN NON-CARDIAC SURGERY operations; this rate is similar to the 12% risk noted in 7 combined series (4, 7, 8, 17, 24, 32, 52) of a total of 1475 thoracic operations between 1955 and 1973. Overall, we noted new SVT's in 4% of our patients, but this is surely an under- estimate because patients were not routinely monitored throughout the postoperative course. Most of the observed postoperative SVT's were coincident with major medical problems which were of a primary cardiac nature only one-third of the time. If analysis is limited to intraoperative ar- rhythmias, Vanik’s epic study (57) of over 5000 patients, half of whom were over the age of 40, with continuous electrocardiographic monitor- ing showed that nodal rhythm, which devel- oped in 7%, was the most common abnormal finding. If, however, special attention is fo- cused on the peri-intubation period, the inci- dence of transient nodal rhythm may be from 25% to as high as 50%, especially with halo- thane anesthesia (1). In our series, the anesthe- siologist who performed the intubation was also the one watching the monitor. Since we did not permanently record peri-intubation events, our 7% incidence of intraoperative bradycardias and 4% incidence of recovery room bradycar- dias is probably an underestimate. All brady- cardias in the operating and recovery rooms were transient and did not correlate with any postoperative cardiac complications. Surgery and heart block Vandam (56), in the pre-pacemaker era, re- ported that 6 of 22 patients with chronic com- plete heart block had circulatory arrests in the operating room but none died. In the present era, essentially every patient with complete heart block in the elderly age group would either already have a permanent pacemaker or would routinely receive prophylactic pace- maker therapy preoperatively. More controver- sial has been the management of patients with bifascicular or trifascicular heart block who have been shown by most but not all studies to have a high long-term risk of complete heart block (24, 38, 39, 40, 42). Four recent studies (5, 23, 34, 58), however, have confirmed our find- ings by describing 138 patients with bifascicu- lar block, 25 patients with bifascicular block and prolonged P-R intervals, and 7 patients with bifascicular block and rhythms other than normal sinus who underwent surgery without progression to complete heart block. Digitalis, 365 which at least 18 of the above patients were receiving, did not increase the risk of observed heart block. In the four combined studies, the only patient who developed complete heart block had 2:1 Mobitz II block preoperatively (58). In our series, one patient with new bifasci- cular block and a prolonged PR interval after a recent reinfarction died despite his prophylactic pacemaker. The only episode of documented complete heart block occurred in a patient who had no conduction disturbances on preoperative EKG, Hypertensive reactions to surgery ‘Small series have shown that blood pressure often rises by 20-45 mm Hg during intubation and laryngoscopy for anesthesia (11). Because most patients’ blood pressures are not moni- tored during this brief period, Gal and Cooper- man's report (16) of 3.25% incidence of hyper- tension, which they defined as a systolic blood pressure greater than 190 mm Hg and a dia- stolic pressure greater than 100 mm Hg, is the most generally quoted. We were not able to accurately record blood pressure during intuba- tion, but we did note hypertension in 6% of previously normotensive patients and’17% of those with a history of hypertension. Medical therapy of hypertension, regardless of whether or not it had dropped preoperative blood pres- sure to the normal range, did not protect against postoperative hypertension. The most important correlate of postoperative hyperten- sion was vascular surgery. This correlation with carotid endarterectomy (25, 59) and vascu- lar surgery (46) has been previously reported, but the relationship to abdominal aortic aneu- rysm surgery should be emphasized. However, as noted by Sechzer et al (46), neither hyperten- sion nor labile blood pressure (hypotension and hypertension perioperatively at different times in the same patient) was an independent pre- dictor of any postoperative cardiac complica- tion. The operation and the anesthetic technique In terms of the operation itself, the emergent nature of the procedure seemed more important than the type or length of the operation or the type of anesthesia, and the duration of un- planned hypotension was more important than the degree of the hypotension. Since intraoper- ative hypotension was correlated with cardi- ogenic shock and not with documented intra- 366 operative or postoperative infarction, we can- not determine whether the hypotension is a cause or result of cardiac decompensation. There is impressive experimental evidence that halothane (19, 54) and nitrous oxide (27, 50) depress myocardial contractility and cardiac output. Thus, it is not surprising that heart failure developed for the first time at a rate of 4.3% after general anesthesia, regardless of the anesthetic agent, but never developed after spinal anesthesia. Among patients who had prior heart failure, the heart failure worsened 22% of the time after general anesthesia but never after spinal anesthesia. Although as a group the patients who had general anesthesia had larger operations than those who had spinal anesthesia, spinal anesthesia did not change the likelihood of developing intraopera- tive hypotension or perioperative arrhythmias, and did not significantly reduce the chance of cardiac death. Experimentally, digitalis will reverse the depression induced by thiopental (18) and halothane (19, 48), but in our uncon- trolled observations in a small number of pa- tients, digitalis gave no apparent protection against the development of clinical postopera- tive heart failure. Multivariate analysis While our univariate analysis had identified many one-way correlates of the various cardiac compleations, a more notable finding is that there are eight independently significant corre- lates of the ultimate complication, cardiac death. The importance of a recent preoperative myocardial infarction, an emergency operation, or unplanned intraoperative hypotension has been discussed above. Signs of marked heart failure (third heart sound or jugular venous distention), rhythm other than sinus, age over 70 years, and valvular aortie stenosis all have been noted to have univariate correlations with overall operative mortality (49), but have never before been shown to have significant multivar- iate relationships to perioperative cardiac death in particular. Of note is that we also found PAC’s to be important. Those patients with preoperative PAC’s who died from cardiac causes were all elderly, having major opera- tions, and were frequently medically or surgi- cally unstable; PAC’s in this subgroup of pa- tients may be an indication that the heart will poorly tolerate a complicated operative course. GOLDMAN ET AL. ‘The eighth factor, frequent PVC’s, has not been. previously emphasized in studies of periopera- tive risk. Interestingly, PVC’s did not correlate with observed ventricular tachycardia, but seemed to be a marker of more severe cardiac disease (43 of the 44 patients with frequent, PVC's in our study had other signs of important heart disease). Similarly, evidence in the non- operated population suggests that in the pres- ence of heart disease (20, 37) or a previous myocardial infarction (21, 31, 41) PVC's, espe- cially if frequent, carry an inereased long-term, mortality risk, at least partly because they are a marker of more severe coronary artery steno- sis and ventricular dysfunction (44, 45, 47). After consideration of these eight variables, no other recognizable factors correlated with postoperative cardiac death. It should again be emphasized that those factors which correlate with the long-term development of coronary artery disease (smoking, hyperlipidemia, hy- pertension, left ventricular hypertrophy, glu- cose intolerance), as well as angina, myocardial infarction more than 6 months preoperatively, symptomatic peripheral vascular disease, or controlled congestive heart failure did not pre- dispose to perioperative cardiac death. SUMMARY In an attempt to assess cardiac risk in non- cardiac surgery, 1001 patients over 40 years of age who underwent major operative procedures were examined preoperatively, observed through surgery, studied with at least one post- operative electrocardiogram, and followed until hospital discharge or death. Documented post- operative myocardial infaretion occurred in only 18 patients; though most of these patients had some pre-existing heart disease, there were few preoperative factors which were statisti- cally correlated with postoperative infarction. Postoperative pulmonary edema was strongly correlated with preoperative heart failure, but 21 of the 36 patients who developed pulmonary edema did not have any prior history of heart, failure. Nearly all of these 21 patients were elderly, had abnormal preoperative electrocar- diograms, and had intraabdominal or intra- thoracic surgery. In the absence of an acute infarction, bifascicular conduction defects, with or without PR interval prolongation, never pro- gressed to complete heart block. Spinal anes- thesia protected against postoperative heart CARDIAC RISK FACTORS IN failure but not against other cardiac complica- tions. By multivariate regression analysis, postoperative cardiac death was significantly correlated with (a) myocardial infarction in the previous 6 months; (b) third heart sound or jugular venous distention immediately preoper- atively; (c) more than five premature ventricu- lar contractions per minute documented at any time preoperatively; (4) rhythm other than sinus, or premature atrial contractions on pre operative electrocardiogram; (e) age over 70 years; (f) significant valvular aortic stenosis; (g) emergency operation; (h) a 33% or greater Appendix. Univariate Correlations of Some Cardia NON-CARDIAC SURGERY 367 fall in systolic blood pressure for more than 10 minutes intraoperatively. Notably unimpor- tant factors included smoking, glueose intoler- ance, hyperlipidemia, hypertension, peripheral atherosclerotic vascular disease, angina, and distant myocardial infarction ACKNOWLEDGMENTS ‘The authors are especially indebted to Alexander. Leaf, M.D. and David Cullen, M.D. We would al like to thank Edgar Haber, M.D.; Barry L. Zaret, M,D.; Peter Yurchak, M.D.; and the attending and resident surgeons who allowed us to study their patients, 1c Risk Factors with Postoperative Infarction and Cardiac Death Risk factor pieat, No witheperperacive No. cardiac deaths Age Less than 70 years nt 6am 30.4%) More than 70 years BA IR 4%) p< Ol 16%) p< 001 Angina: No 8501809) Bam ? 69 34%) NS 2am) NS. Yes, stable 0 2a%) NS. aaa) NS Ischemia by history or EKG: No m2 Ra sum Yes 269 TaQ%) NS 114%) p<.005 Hypertension: Never eam 2ew® Yes, normal on treatment 127 sum) NS. 40%) NS Yes, no treatment 9 10% NS. 22%) NS. Yes, high despite treatment 6 o NS. 1Q% NS. Shortness of breath, orthopnea, or edema: No 75 6%) 70%) Probably "Non-Cardiac” 160, 114%) p= 01 413%) NS, “Cardiac” 115 514%) p= Ol 716%) p<.001 History heart failure. No 865 132m) nas Yes 108 30% NS 44%) NS. Pulmonary edema 2 20%) NS 304%) p< 001 Heart failure status. Never 83am) 120% In past, not now 86 3m) NS 415%) N Now 66 20%) NS a6) p= ugular venous distention. No 162%) Bus 2 10%) NS. 113%) Yes Lag) NS. 522%) ‘All significance t ing was by Chi-square analysis wi ith Yates correction comparing those patients with & particular abnormal characteristic to those in whom the characteristic was normal or not present. Note that full historical information could not be obtained on all " indeterminate intraventricular conduction delay. * Jet anterior hemiblock * eft bundle branch block. * right bundle branch block. patients. Appendix— Continued ia Tar a Ri sao, No. cardia deaths Rates. No s% 192%) 90% ? Cardiac 142 20%) NS. 75%) p<.01 Cardiac 10%) NS 26%) NS. (Any rales) (176) 3%) N.S. 915%) p< .01 Se gallop No s9 12%) new Yes a4 40%) NS 70m) NS. Palpable B 16%) NS. Oae 5 S; gallop: No ew 16 2%) Yes 7 16%) NS, 3.18%) p<.001 Rhythm: Normal sinus 0s 17%) baw Atrial fibrillation 48 0 NS. 3 (6%) p= .06 Other 7 16% NS. 308%) p<.001 Premature atrial beats now: No 98 6a% 14 @%) Yes 24%) NS. 518%) p<.001 Ever more than five premature ventricular beats per minute No 7 4a 130.4%) Yes 4%) p<.o 644%) p<.oo1 QRS: Normal 709 10%) wan) Ivcp' 38 25%) NS. 308%) p< .05 LAHB* 90 4(4%) NS. 11%) N.S. LBBB* 20 0 N.S. 1(5%) N.S. RBBB: 310%) NS 26%) N. RBBB & LAHB % 0. NS 219%) (All abnormal) (202) 73%) NS. 9 (5%) ST segments: Normal sm 70%) 40% Cannot clasify uo NS 319%) p<.oo1 Nonspecific 6am) NS. 80%) p<.0s Abnormal, from digitalis or electrolytes 25 14%) N.S. 2 (8%) p< .05 Ischemic 2 40%) NS 20%) NS. (All abnormab 43) 12.26%) NS. Bam p

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